Dislocation and degradation from the ER are regulated by cytosolic stress.
Dislocation and degradation from the ER are regulated by cytosolic stress.
复制标题
DOI：
10.1083/jcb.200111045
复制
发表时间：
2002-04-29
期刊：
影响因子：
--
通讯作者：
Musil LS
中科院分区：
文献类型：
--
作者：
VanSlyke JK;Musil LS
Akey step in ER-associated degradation (ERAD) is dislocation of the substrate protein from the ER into the cytosol to gain access to the proteasome. Very little is known about how this process is regulated, especially in the case of polytopic proteins. Using pulse-chase analysis combined with subcellular fractionation, we show that connexins, the four transmembrane structural components of gap junctions, can be chased in an intact form from the ER membrane into the cytosol of proteasome inhibitor–treated cells. Dislocation of endogenously expressed connexin from the ER was reduced 50–80% when the cytosolic heat shock response was induced by mild oxidative or thermal stress, but not by treatments that instead upregulate the ER unfolded protein response. Cytosolic but not ER stresses slowed the normally rapid degradation of connexins, and led to a striking increase in gap junction formation and function in otherwise assembly-inefficient cell types. These treatments also inhibited the dislocation and turnover of a connexin-unrelated ERAD substrate, unassembled major histocompatibility complex class I heavy chain. Our findings demonstrate that dislocation is negatively regulated by physiologically relevant, nonlethal stress. They also reveal a previously unrecognized relationship between cytosolic stress and intercellular communication.
登录
查看更多内容
FGF和细胞外信号调节激酶在透镜中的细胞间通信中的新作用。
影响因子：
7.8
作者：
Le, A C;Musil, L S
通讯作者：
Musil, L S
DOI：
10.1083/jcb.131.5.1193
发表时间：
1995-12
期刊：
The Journal of cell biology
影响因子：
--
作者：
Laird DW;Castillo M;Kasprzak L
通讯作者：
Kasprzak L
影响因子：
5.6
作者：
LEE, YJ;DEWEY, WC
通讯作者：
DEWEY, WC
影响因子：
4.8
作者：
Mancini, R;Fagioli, C;Sitia, R
通讯作者：
Sitia, R
影响因子：
20.1
作者：
Beardslee, MA;Laing, JG;Saffitz, JE
通讯作者：
Saffitz, JE